摘要
目的研究急性左心衰竭(ALHF)患者的炎性介质变化、T淋巴细胞亚群、NK细胞的表达及与NYHA分级的关系,为临床治疗提供新的思路。方法选择符合AuIF标准38例患者为试验组(B组),根据NYHA分级分为心功能Ⅱ级组和心功能Ⅲ、Ⅳ级组两个亚组;同期健康查体并排除器质性疾患志愿者30例作为对照组(A组),运用流式细胞仪测定外周血清T淋巴细胞亚群(CD3+、CD4+、CD8+、CD4+/CD8+)、NK;ELISA法监测CRP、TNF-α}表达水平,分析上述指标变化与NYHA分级的关系;试验数据采用PEMS统计软件包进行统计学分析。结果试验组CD3+、CD4+、CD4+/CD8+及NK明显降低,与对照组比较差异有统计学意义(均P〈0.05),CD8+、CRP及TNF一仪明显升高,与对照组比较差异有统计学意义(均P〈0.01)。在NYHAⅢ、Ⅳ级的患者中,其变化更显著,与NYHA11级患者比较差异有统计学意义(P〈0.05)。结论ALHF患者的细胞免疫功能下降,表现为CD3+、CD4+、CD4+/CD8+及NK下降,CD8+升高;CRP和TNF-α升高,故调整细胞免疫功能和调控炎性介质可能是ALHF患者的治疗新思路。
Objective To investigate the expression of T cellular immune, NK cells, inflammation factors ( CRP, TNF - α) in patients with acute left heart failure, and the relationship with the NYHA. Methods 38 patients with ALHF were test group, flow cytometry was applied for assessing proportions of CD3 + T cells, CD4+ T cells, CD8 + T cells, CIM+/CD8 + ratio, NK cells in the vain serum, at the moment, there was some other serum that was used for testing CRP level and TNF - α level. Obstruct the association among these factors with the NYHA grade. Simuhaneously, 30 healthy individuals served as normal group. The data was analyzed with the PEMS system. Results Compared with normal group, the level of CD3 + , CD4 + , CD4 +/CD8 + ratio and NK decreased sharply, with a statistical difference ( P 〈 0.05). The level of CD8 + , CRP and TNF - α increased sharply, and had a statistical difference compared with normal group( P 〈 0.01 ). There was a sharply change between the patients with NYHA Ⅲ、Ⅳ and NYHA Ⅱ ( P 〈 O. 05). Ulteriorly, there were also association with the prognosis. Conclusion Immunity lessen in patients of ALHF, especially the lever of CD3+ , CD4 + , CD4 +/CD8+and NK, but the lever of CD8+ , CRP and TNF -α increased. So, regulation of immunity and inflammation may be a new way of ALHF treatment.
出处
《中国急救医学》
CAS
CSCD
北大核心
2012年第6期491-493,共3页
Chinese Journal of Critical Care Medicine
基金
贵州省科技攻关项目(黔科合S字[2007]1052)
关键词
急性左心衰竭(ALHF)
免疫调节
炎性介质
细胞免疫
Acute left heart failure(ALHF)
Immune mediate
Inflammatiory mediators
Cell - mediated immunity